Acute severe Asthma is a common paediatric emergency managed according to the BTS and SIGN guidelines. They recommend that if initial β2 agonist treatment bears no response, frequent Ipratropium Bromide doses can be given every 20-30 minutes [1]. We present a case of paradoxical bronchospasm to Ipratropium, an observed but rare side effect. Case ReportAn eight-year-old girl presented to the Emergency Department with cough and shortness of breath. Her asthma was usually well controlled with Beclamethasone 100 micrograms twice-daily, Montelukast once-daily, and Salbutamol as and when required. She had no history of rhinoconjunctivitis nor any allergic triggers. She was diagnosed with an acute non-infectious exacerbation of Asthma and given ten puffs of Salbutamol inhaler every 20 minutes over one hour. As she showed marked symptomatic improvement, she required no investigation and was discharged with a wheeze plan and oral amoxicillin cover for seven days. However, she returned that evening with increasing breathlessness and an audible wheeze on auscultation. She was then started on ten puffs Salbutamol MDI, two puffs Ipratropium Bromide inhaler 20 microgram via spacer and Prednisolone 40 mg. She responded to the treatment and Salbutamol was gradually spaced to four-hourly. The next day she was discharged with a three-and seven-day course of Prednisolone and Amoxicillin to complete, respectively.
The role of bronchodilators in lung disease was investigated. It was found that 90% of patients sent for lung function tests have obstructive airways disease. Of these, 75% benefited from inhalation of a bronchodilator, the average improvement being a 26% increase in FEV1• Examination of the changes in arterial oxygen showed that although there was on the average a small significant drop in arterial oxygen, there were sometimes quite significant rises too. The falls tended to occur from high arterial oxygen pressures, while those who had low resting values showed a small fall, no change or even a rise in Pao2. These changes correlated with indirectly initiated changes in alveolar ventilation, an increased alveolar ventilation tending to cause a decrease in arterial oxygen and vice versa.The mechanism for this is thought to be part of the control of ventilation perfusion matching, for even in normals made to hyperventilate there is a widening of the alveolar:arterial oxygen gradient as the Paco2 falls.
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